Massive intracerebral hemorrhage following carotid endarterectomy

To our knowledge, a particularly lethal complication of carotid endarterectomy, intracerebral hemorrhage, has not been given due consideration in the literature concerning carotid surgery. In the Atlanta area, massive intracranial hemorrhage developed in ten patients following routine carotid endarterectomies performed during a recent ten-year period. All ten of the patients in this series died despite a variety of therapeutic interventions. Risk factors may include the following: extreme arterial stenosis with resultant postoperative hyperperfusion, involvement of multiple extracranial cerebral vessels, postoperative systemic hypertension, and administration of anticoagulant or antiplatelet medications. Unfortunately, identification of the subset of patients potentially at risk for this complication is difficult, and, to date, therapy has been generally ineffective.     

Incidence and etiology of intracerebral hemorrhage following carotid endarterectomy

In a consecutive series of 1930 carotid endarterectomies there were eight cases of postoperative intracerebral hemorrhage. One of these patients was operated on 2 weeks following cerebral infarction and had severe uncontrollable hypertension after surgery. A second patient had an intraoperative embolus and bled while fully heparinized on the 3rd postoperative day. Only one patient in the series bled into an area of documented cerebral infarction. The remainder of the cases represented hemorrhage into essentially normal brain. Seven of the eight patients with intracerebral hemorrhage had high-grade internal carotid artery stenosis preoperatively. Although several factors have contributed to the brain hemorrhages in this series of patients, postoperative cerebral hyperperfusion which often follows endarterectomy may have played an important role. Defective cerebrovascular autoregulation in chronically ischemic brain regions may predispose patients to intracerebral hemorrhage after removal of a high-grade stenosis of the internal carotid artery.     

Mechanisms of intracerebral hemorrhage after carotid endarterectomy.

OBJECT: Intracerebral hemorrhage (ICH) is an uncommon complication of carotid endarterectomy (CEA), and carries a high rate of mortality and morbidity. Traditionally, attention has been focused on the cerebral hyperperfusion syndrome (HPS) as the leading cause of ICH after CEA. Other mechanisms, such as a perioperative cerebral ischemic event, cerebral infarction, and use of postoperative anticoagulation therapy, may also be important. METHODS: The authors performed a retrospective case control study to identify factors leading to ICH after CEA. Records of CEAs performed over the past 10 years at the Mayo Clinic were searched for occurrences of ICH within 30 days of the procedure. The relationship of ICH to known cerebrovascular risk factors, perioperative electroencephalographic studies, and 133Xe cerebral blood flow (CBF) studies was compared with that in a control group. Hyperperfusion was defined as hypertension with symptoms of either severe headache, seizures, or confusion, or a doubling of intraoperative CBF values. The clinical history and imaging of ischemic events and the ICH were carefully reviewed to determine the possible underlying mechanism(s). Twelve (0.4%) of 2747 patients who underwent CEAs suffered a postoperative ICH. A doubling of CBF values was found in five of eight cases in which CBF studies were performed, and occurred more commonly in the patients with ICH than in controls. Clinical symptoms of the HPS were less common (three cases). A perioperative cerebral ischemic event (four cases) and anticoagulation therapy (six cases) were other contributors to a subsequent ICH. Seven of the 12 patients with ICHs died and five achieved a moderate outcome. CONCLUSIONS: An ICH following CEA is an unusual complication that occurs in the setting of hyperperfusion, perioperative cerebral ischemia, anticoagulation therapy, or multiple mechanisms. Identification of CBF doubling at surgery may assist in identifying patients at risk for ICH following CEA.     

Myocardial infarction following carotid endarterectomy: a review of 683 operations.

In a series of 683 consecutive carotid endarterectomies, there were 16 postoperative myocardial infarctions which resulted in five deaths. Of 399 operations on patients with no previous history of heart disease, there were only two myocardial infarctions (0.5%). Two hundred and eighty-four operations were performed on patients with heart disease, and vasopressors were administered in 135 of these procedures. For these patients the risk of myocardial infarction increased from 2.0% to 8.1% with the use of vasopressors (P less than 0.001). The management of the patient with stable heart disease undergoing carotid endarterectomy is discussed.     

Hypertension following carotid endarterectomy.

Seventy-nine patients undergoing staged bilateral carotid endarterectomy were studied to determine the relationship of perioperative hypertension to postoperative neurologic deficits. Six of the eight neurologic deficits following 158 endarterectomies (5%) occurred after the first operation, all being temporary. Comparison of the mean blood pressures in patients with and without postoperative strokes revealed no statistically significant differences. Patients on antihypertensive medications were at a significantly higher risk of developing postoperative strokes. A trend towards higher blood pressure was noted following the second endarterectomy, particularly when they were staged more than 60 days apart. Based on our findings, a cautious approach is warranted in the treatment of postendarterectomy hypertension.     

Intracerebral haemorrhage following carotid endarterectomy.

OBJECTIVES: To determine risk factors for the development of hyperperfusion and intra-cerebral haemorrhage following carotid endarterectomy and formulate potential protocols for prevention. METHODS: MEDLINE database search of the English language literature (1966-2002) was performed using the words 'cerebral haemorrhage', 'intracranial haemorrhage' and 'carotid endarterectomy'. Other articles were cross-referenced by hand. RESULTS: There are no data from randomised trials confirming the significance of any single risk factor. The evidence suggests that the following may have a role: pre-operative hypertension, recent ipsilateral non-haemorrhagic stroke, previous ischaemic cerebral infarction, surgery for a > 90% ipsilateral internal carotid artery (ICA) stenosis, impaired cerebrovascular reserve, intra-operative haemodynamic or embolic ischaemia, post-operative hypertension, an ipsilateral increase of > or =175% in peak middle cerebral artery velocity (MCAV) and/or a > or =100% increase in pulsatility index. CONCLUSIONS: A critical ICA stenosis with impaired cerebrovascular reserve resulting in maximal intracerebral vasodilatation and post-operative hyperperfusion (impaired autoregulation) appear to be central to the development of ICH. Appropriate pre-operative screening and post-operative monitoring in high risk patients might identify those who would benefit from manipulation of the haemodynamic events that appear to promote ICH.     

Complications following carotid endarterectomy for all indications: report of 192 operations

The complications (stroke, myocardial infarction, and death) with 192 endarterectomies performed on 162 patients were evaluated and categorized according to the presenting syndrome: asymptomatic bruit, transient ischemic attack, stroke, stroke in progress, and posterior fossa ischemia. Each group's complication rate was then evaluated over several postoperative periods (0.5 hour to 30 days) and compared with rates in comparable studies. Overall mortality for the entire series was 0.5%. This study points out the need to separate patients having undergone endarterectomy into presenting groups before comparing with other studies having similar postoperative observations.     

Recurrent carotid artery stenosis following endarterectomy.

Spectral analysis was used to examine 257 carotid arteries in 227 patients who had undergone carotid endarterectomy at 1, 3, 6, and 12 months after surgery and annually thereafter. Routine intraoperative completion angiography ensured that the operations were technically satisfactory. Postoperative restenoses were identified in 38 patients (15%). In 23 arteries (9%), the restenosis exceeded a 50% diameter reduction while in 15 arteries (6%) the stenosis was less than 50% of the diameter. Restenosis developed in 24/96 women (25%) and 14/161 men (9%). Twenty-nine (70%) stenotic lesions occurred within 12 months. In three patients early lesions regressed. Reoperation with patch angio-plasty was required in six patients. When the 219 carotid arteries that remained widely patent were compared to the 38 that restenosed , no differences were noted for age, diabetes mellitus, hypertension, smoking, or degree of preoperative stenosis. Early stenotic lesions appear to be due to myointimal hyperplasia, which is probably platelet mediated. The predominant female sex distribution may be explained by differences in platelet responsiveness in men and women.     

Motor speech deficit following carotid endarterectomy.

Stroke as a complication of carotid endarterectomy has been extensively reviewed. Considerably less attention has been directed to local injuries of the cranial nerves and their branches. Verta, Hertzer, Imparato, DeWeese, and Matsumoto have reported experience with these injuries. DeWeese found a 9.7% rate of cranial nerve injury, while in Hertzer's series, 15% of patients had nerve dysfunction in the early postendarterectomy period. In 1980, Liapis in a preliminary report found that when postoperative examination was supplemented by detailed evaluation by speech pathologists, the incidence of early abnormalities reached 27%. The purpose of this study was to expand upon Liapis' early observation and to clarify the contribution of the speech pathologists in identifying cranial nerve dysfunctions, specifically those resulting in motor speech abnormalities, following carotid endarterectomy.     

Spontaneous intracerebral hemorrhage in cases of severe angiospasm following ruptured aneurysm--a pathological study.

Eleven patients with a history of moderate or severe angiospasm following ruptured cerebral aneurysm developed spontaneous intracerebral hemorrhage between 31 and 111 months after aneurysm surgery. In all cases, hemorrhage occurred in the ipsilateral hemisphere to the original aneurysm. In nine patients, the hematoma was surgically evacuated and bleeding perforating arteries were resected for histological examination. Computed tomographic scans showed the hematomas to be unusually extended compared to those after hypertensive intracerebral hemorrhage. The histological examination showed various degenerative changes in the elastic lamina and media of the perforating arteries, even though most patients were young and normotensive. These findings suggest that patients who have suffered severe cerebral angiospasm may have a higher risk for subsequent development of intracerebral hemorrhage than those without prior angiospasm.     

Vascular reconstruction following trauma. Experience in Basel 1980-1988

From 1980-1988 twenty patients with vascular trauma were treated at the Kantonsspital Basel, Switzerland. The incidence of 1% in open fractures is low. Nerve lesions in combination with vascular trauma are very frequent, specially at the upper extremity. Nearly all patients were treated with the interposition of a venous graft from the vena saphena magna. We deplore 3 amputations after successful vascular reconstruction, mainly due to extensive bone and soft tissue damage. Our long-term control shows very satisfying vascular results, but poor neurological results. We therefore conclude that the functional outcome is--apart from a short ischemia time--highly related to the neurological situation at the time of the trauma.     

Control of hypertension following carotid endarterectomy

The role of carotid endarterectomy in the treatment of extracranial carotid artery disease has been well established. Postoperative hypertension is a significant prognostic factor and is associated with an increased incidence of both transient and permanent neurologic deficits. We studied 110 patients undergoing unilateral carotid endarterectomy to review the efficacy of the drug combination of hydralazine and propranolol to treat postoperative hypertension. All patients receiving hydralazine and propranolol had their blood pressure controlled postoperatively, and no patients developed hypotension, myocardial infarction, or postoperative neurologic deficits. There were no mortalities in the study group. We conclude that propranolol-hydralazine therapy is a safe and effective means to control hypertension associated with carotid endarterectomy.     

Restenosis following carotid endarterectomy. Evaluation by duplex ultrasonography

This study evaluated the efficacy of duplex ultrasonographic scanning in assessing the status of carotid arteries after 155 endarterectomies in 131 patients. Duplex studies were done as early as one month and as late as 96 months postoperatively; 33 patients had serial studies. Only 59 (42%) of 142 arteries had no evidence of irregularity or reduction in diameter at the operative site. An additional 41 (29%) had a reduction in diameter between 10% and 29%; 19 (13%) had reductions of 30% to 49%; nine (6%) from 50% to 69%; six (4%) from 70% to 99%; and eight (6%) were occluded. In 51 vessels, angiographic studies confirmed the duplex findings. Symptoms suggestive of recurrent cerebrovascular disease occurred postoperatively in 25 instances; in only three were the anatomic findings suggestive of lesions appropriate to the symptoms. We conclude that duplex ultrasonographic scanning is a useful technique for assessing carotid arteries after endarterectomy and that postoperative narrowing of vessels occurs more commonly than suspected.     

Stenosis following carotid endarterectomy. Its implication in management of asymptomatic carotid stenosis

Carotid endarterectomy is established in the treatment of atherosclerosis of the carotid bifurcation, but the incidence of restenosis and the role of endarterectomy in the management of asymptomatic carotid stenosis are variable. During a four-year period, we performed 80 endarterectomies of the internal carotid artery in 73 patients. Patients were prospectively studied by means of Doppler ultrasonography in combination with real-time spectral analysis to determine the incidence of restenosis postoperatively. A concomitant study of 116 patients with 79 asymptomatic carotid stenoses was undertaken. We found a 12.5% incidence of stenosis following carotid endarterectomy and a 3% risk of transient neurologic deficit in the patients with asymptomatic carotid stenoses.     

Risk prediction of outcome following carotid endarterectomy

The quoted combined mortality and morbidity following carotid endarterectomy is about 5–7%. In an attempt to identify a subgroup of high risk patients, a review has been undertaken of 404 carotid endarterectomies performed between January 1985 and March 1994. The perioperative mortality rate was 2%, with 3.4% of patients experiencing transient neurological deficits and 4% permanent strokes. Multiple logistic regression analysis was used to estimate the influence on outcome of age, gender, indication for surgery, bilateral internal carotid artery disease, hypertension and smoking. No significant explanators were identified.     

Management of acute postoperative thrombosis following carotid endarterectomy

We reviewed 326 carotid endarterectomies performed from 1960 through 1981 and encountered five instances of acute postoperative thrombosis. Clinical decompensation occurs with the acute onset of severe neurologic deficits, most characteristically dense hemiplegias contralateral to the side that has been operated on. These deficits developed between two and 72 hours postoperatively. Prompt reoperation with thrombectomy and reestablishment of carotid flow within two hours from the onset of the neurologic deficit was performed on four patients with complete resolution of the deficits in three patients. The fourth patient recovered from a severe hemiplegia but retained a slight residual weakness of the hand. The one patient whose condition did not improve underwent thrombectomy more than 24 hours after the onset of her deficit. Time-consuming diagnostic procedures are not warranted as the success of reoperation depends on rapid reestablishment of cerebral flow.